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Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life
INTRODUCTION: Silica nanoparticles (SiO(2)-NPs) are currently among the most widely used nanomaterials, but their potentially adverse effects on brain development remain unknown. The developing brain is extremely sensitive to NP neurotoxicity during the early postnatal period. MATERIALS AND METHODS:...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6018854/ https://www.ncbi.nlm.nih.gov/pubmed/29950837 http://dx.doi.org/10.2147/IJN.S160828 |
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author | Fu, Jingjing Gao, Junwei Gong, Linji Ma, Yuanyuan Xu, Haiwei Gu, Zhanjun Zhu, Jingci Fan, Xiaotang |
author_facet | Fu, Jingjing Gao, Junwei Gong, Linji Ma, Yuanyuan Xu, Haiwei Gu, Zhanjun Zhu, Jingci Fan, Xiaotang |
author_sort | Fu, Jingjing |
collection | PubMed |
description | INTRODUCTION: Silica nanoparticles (SiO(2)-NPs) are currently among the most widely used nanomaterials, but their potentially adverse effects on brain development remain unknown. The developing brain is extremely sensitive to NP neurotoxicity during the early postnatal period. MATERIALS AND METHODS: Herein, we investigated the effects of SiO(2)-NPs (doses of 10, 20, or 50 mg with a particle size of ~91 nm, equivalent to aerosol mass concentrations 55.56, 111.11, and 277.78 mg/m(3), respectively) exposure from postnatal day (P) 1 to P7 on hippocampal precursor proliferation at P8 and long-term neurobehavior in adults. RESULTS: SiO(2)-NP exposure resulted in inflammatory cell infiltration in lung tissue, microglia over-activation in the hippocampal dentate gyrus (DG), and decreased hippocampal precursor proliferation in the DG-subgranular zone at P8. Moreover, after exposure to 20 mg of SiO(2-)NPs, mice exhibited social interaction deficits and slight anxiety-like behaviors in adulthood, but this exposure did not induce locomotor activity impairment, depression-like behavior, or short-term memory impairment. DISCUSSION: These findings suggest that early-age SiO(2)-NP exposure induced inflammation and inhibited precursor proliferation in the DG in a dose-dependent manner, which might be related to the social dysfunction observed in adulthood. |
format | Online Article Text |
id | pubmed-6018854 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-60188542018-06-27 Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life Fu, Jingjing Gao, Junwei Gong, Linji Ma, Yuanyuan Xu, Haiwei Gu, Zhanjun Zhu, Jingci Fan, Xiaotang Int J Nanomedicine Original Research INTRODUCTION: Silica nanoparticles (SiO(2)-NPs) are currently among the most widely used nanomaterials, but their potentially adverse effects on brain development remain unknown. The developing brain is extremely sensitive to NP neurotoxicity during the early postnatal period. MATERIALS AND METHODS: Herein, we investigated the effects of SiO(2)-NPs (doses of 10, 20, or 50 mg with a particle size of ~91 nm, equivalent to aerosol mass concentrations 55.56, 111.11, and 277.78 mg/m(3), respectively) exposure from postnatal day (P) 1 to P7 on hippocampal precursor proliferation at P8 and long-term neurobehavior in adults. RESULTS: SiO(2)-NP exposure resulted in inflammatory cell infiltration in lung tissue, microglia over-activation in the hippocampal dentate gyrus (DG), and decreased hippocampal precursor proliferation in the DG-subgranular zone at P8. Moreover, after exposure to 20 mg of SiO(2-)NPs, mice exhibited social interaction deficits and slight anxiety-like behaviors in adulthood, but this exposure did not induce locomotor activity impairment, depression-like behavior, or short-term memory impairment. DISCUSSION: These findings suggest that early-age SiO(2)-NP exposure induced inflammation and inhibited precursor proliferation in the DG in a dose-dependent manner, which might be related to the social dysfunction observed in adulthood. Dove Medical Press 2018-06-22 /pmc/articles/PMC6018854/ /pubmed/29950837 http://dx.doi.org/10.2147/IJN.S160828 Text en © 2018 Fu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Fu, Jingjing Gao, Junwei Gong, Linji Ma, Yuanyuan Xu, Haiwei Gu, Zhanjun Zhu, Jingci Fan, Xiaotang Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title | Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title_full | Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title_fullStr | Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title_full_unstemmed | Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title_short | Silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
title_sort | silica nanoparticle exposure during the neonatal period impairs hippocampal precursor proliferation and social behavior later in life |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6018854/ https://www.ncbi.nlm.nih.gov/pubmed/29950837 http://dx.doi.org/10.2147/IJN.S160828 |
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